Effect of ECT on the neuroendocrine response to apomorphine in severely depressed patients.
Animal studies have suggested that the mechanism of the antidepressant action of ECT may be to increase monoaminergic post-synaptic receptor sensitivity. We have tested this hypothesis in 12 drug-free patients suffering from severe depression, 11 of whom had depressive delusions. The responses of growth hormone, prolactin and cortisol to 0.75 mg subcutaneous apomorphine were examined before and after a successful course of ECT. There were no significant differences between hormonal measurements on the two occasions, with the exception that basal plasma cortisol concentrations were significantly lower following ECT and recovery from depressive illness. These results do not support the hypothesis that ECT increases dopaminergic post-synaptic receptor sensitivity.
D000328:Adult; D000368:Aged; D001058:Apomorphine; D003866:Depressive Disorder / Q000097:blood* / Q000628:therapy; D004565:Electroconvulsive Therapy; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D013006:Growth Hormone / Q000097:blood; D006728:Hormones / Q000097:blood*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D011388:Prolactin / Q000097:blood; D013972:Thyrotropin / Q000097:blood
D006728:Hormones; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone; D001058:Apomorphine; D006854:Hydrocortisone